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Renal > Chronic Kidney Disease I and II > Flashcards

Chronic Kidney Disease I and II Flashcards

1
Q

Chronic Kidney Disease Definition

A

•The presence of either kidney damage or decreased kidney function for > 3 months with or without decreased glomerular filtration rate (GFR)

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2
Q

Clinical Markers of Kidney Damage

A
  1. Proteinuria: >150mg per day of protein in the urine
    a. Albumin is most prominent component of protein in the urine and is often measured in lieu of the total protein - >30mg of albuminuria per day is abnormal
  2. Glomerular hematuria: dysmorphic red blood cells (RBCs) or red blood cell casts on urinary sediment review –> indicates glomerular origin – glomerular disease Dysmorphic RBCs RBC cast c.Imaging: Polycystic kidneys, hydronephrosis, or small kidneys with thinned cortex on ultrasound
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3
Q

Decreased Kidney Function

A

a. GFR < 60ml/min/1.73 m2 for > 3 months (remember normal GFR is between 90-120ml/min)
b. Need to document at least 2 measurements separated by at least 2 weeks

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4
Q

GFR Measurement

A
  • serum creatinine
  • creatinine clearance
  • estimated GFR - Modifications of DIet and Renal Disease (MDRD) equation
  • Chronic Kident=y Disease Epidemiology Collaboration Equation (CKD-EPI)
  • cystatin C
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5
Q

Serum Creatinine

A
  1. Derived from the metabolism of creatine in skeletal muscle and from dietary meat intake
  2. Released into the circulation at a relatively constant rate and has a stable plasma concentration
  3. Freely filtered across the glomerulus and is neither reabsorbed nor metabolized. It is inversely proportional to GFR
  4. Can only be used in patients with stable kidney function
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6
Q

Limitations of Serum Creatinine

A
  1. Not accurate in patients with little muscle mass (liver disease, malnourished patients, congenital dwarfism, etc) – may have a creatinine within normal range but have a significant reduction in GFR (generate less creatinine from decreased muscle mass)
  2. Also secreted by organic secretory pathway in the proximal tubule i. Certain medications can inhibit the secretion of creatinine (TrimetheprimSulfamathoxazole, Cimetadine) and increase serum creatinine despite no change in GFR
  3. Does not detect early changes in GFR
  • An initial small rise in serum creatinine reflects a marked change in GFR whereas a marked rise in serum creatinine with advanced disease reflects a small absolute reduction in GFR
  • i.e. A decline in GFR from 120 to 80mL/min per 1.73m2 (loss of 40mL/min) in a 70Kg gentleman is associated with only a small rise in serum creatinine from 0.9 to 1.0 (because of increased creatinine secretion* - more creatinine is secreted into the tubule with early changes in GFR)
  • A further elevation in serum creatinine to 1.5mg/dL represents the loss of at least 1/3 or 27mL/min of the remaining GFR (assuming there is no further creatinine secretion)
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7
Q

Creatinine Clearance

A
  • Clearance = UV/P where U=urinary concentration of a substance, V=volume of urine per set time (in this case 24h), and P=plasma concentration of a substance
  • Because creatinine is filtered and not reabsorbed by the tubule, we can measure the clearance of creatinine to obtain the measurement of GFR
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8
Q

Creatinine Clearance Limitations

A

Limitations:

a. Remember – creatinine is also secreted into the tubule. Therefore the urinary creatinine concentration will be higher than what was actually filtered –> creatinine clearance will exceed the true GFR by ~ 10-20%
b. Inaccurate collection - patients notoriously will over-collect (>24h) or under-collect urine
c. Because of these limitations, creatinine clearance is no longer recommended for routinely assessing GFR

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9
Q

Estimated GFR

A
  1. Estimates GFR by incorporating known demographic and clinical variables as observed surrogates for unmeasured factors other than GFR that affect serum creatinine a. i.e. age, gender, ethnicity, in addition to creatinine b. Actual formula is long and complicated – you are not responsible for it!
  2. Increasingly used not only to estimate GFR but follow changes in GFR
  3. Becomes less accurate when GFR >60ml/min/1.73m2
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10
Q

CKD-EPI

A
  • Also estimates GFR based on age, gender, ethnicity, and creatinine.
  • Better accuracy than MDRD when GFR >60ml/min (may eventually replace MDRD; for now MDRD is used most often in the US)
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11
Q

Cystatin C

A

•Alternative endogenous filtration marker that may have advantages over creatinine for GFR estimation ( not ready for prime time yet)

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12
Q

Stages of Chronic Kidney Disease

A

•Staging kidney disease identifies patients who are at highest risk for progression and having complications from chronic kidney disease

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13
Q

CAuses of Chronic Kidney Disease

A
  • Tubulointerstitial
  • Vascular
  • Glomerular
  • Post Renal
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14
Q

Tubulointerstitial Disease

A
  1. Polycystic kidney disease
  2. Autoimmune diseases
  • Sjogren’s disease, Sarcoidosis
  • Inflammatory infiltrate in the interstitium with associated tubular dysfunction
  1. Reflux nephropathy (vesicoureteral reflux)
  • Passage of urine from the bladder into the upper urinary tract
  • Typically due to inadequate closure of the ureterovesical junction
  • Presents in childhood
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15
Q

Vascular Disease

A
  1. Hypertensive vasculopathy or benign nephrosclerosis (due to hypertension)
  2. Renovascular disease

•Due to either bilateral or unilateral renal artery stenosis (atherosclerotic plaque or fibromuscular dysplasia that reduces renal arterial blood flow)

  1. Renal atheroembolic disease (cholesterol emboli)

• Many patients do NOT recover full function after an event ultimately resulting in CKD

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16
Q

Glomerular Disease

A
  1. Diabetic nephropathy (the most common cause of CKD in the United States)
  2. Primary glomerular diseases
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17
Q

Post Renal or Obstructive Uropathy

A

If obstruction is prolonged without intervention, parenchymal loss will result (loss of nephron mass due to compression from reflux of urine)

  1. Benign prostatic hyperplasia (most common)
  2. Urethral strictures
  3. Chronic obstructive calculi (nephrolithiasis)
  4. Pelvic masses (external compression on ureters)
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18
Q

Acute KIdney Injury

A

Chronic sequelae from having either an initial or repeated episodes of AKI is increasingly recognized as a cause for CKD

19
Q

Pathophyisiology of Chronic Kidney Disease

A

Regardless of underlying disease, it is thought that the final common pathway to progressive CKD is shared mechanism

  1. Initial insult to the kidney (i.e. tubulointerstitial, vascular, glomerular, or obstructive uropathy) leads to nephron loss
  2. Renal function is initially maintained as the remaining nephrons will hyperfilter (GFR will remain the same)
  3. The ongoing hyperfiltration results in glomerular capillary hypertension (each remaining nephron is under higher pressure given the higher filtering demands)
  4. Glomerular capillary hypertension leads to cytokine activation (cell-signaling proteins) and podocyte dysfunction (glomerular epithelial cells that help maintain capillary loop shape) resulting in:
    a. Proteinuria
    b. Glomerular sclerosis
    c. Tubulointerstitial fibrosis

—> renal scarring

20
Q

Most Commone Diseases That Predispose CKD

A
  • Diabetes Mellitus
  • Hypertension
21
Q

DM

A
  • 20-30% of diabetics will develop diabetic nephropathy
  • accounts for 55% of new dialysis patients
  • Given the increase in prevalence of Type II diabetes compared to Type I, Type II diabetes accounts for the majority of cases of diabetic nephropathy
  • The renal risk for progression of disease (CKD) is equivalent in both Type I and II diabetes
22
Q

Manifestations of DM

A

•Glomerulopathy characterized by mesangial expansion, thickening of the glomerular basement membrane, and glomerulosclerosis

23
Q

Clinical Characteristics of DM

A
  1. Hyperfiltration and glomerular capillary hypertension – this is the earliest clinical manifestation of disease
  2. Microalbuminuria: (now referred to as high albuminuria) – urinary albumin between 30mg-300mg (normal <30 mg per day)
    a. This predicts high risk for future overt nephropathy (> 1 gram of proteinuria)
    b. Crucial for effective therapy to target glomerular capillary hypertension (i.e. ACE inhibitors and angiotensin receptor blockers), glycemic control, and weight control in order to slow or halt the progression of disease!
  3. Macroalbuminuria: (now referred to as very high albuminuria) – urinary albumin >300mg per day
    a. In the absence of effective therapy, patients will have a progressive decline in GFR and ESRD (if they do not die from a cardiovascular related event first!)
  4. Progressive disease with little or no albuminuria:
    a. Subset of diabetic patients that still have progressive CKD but decline in GFR is not related to albuminuria
    b. Thought to be due to intrarenal vascular disease
    c. Rate in decline of GFR is much slower compared to albuminuric patients
24
Q

Pathogenesis of Diabetic Nephropathy

A

• Includes glomerular hyperfiltration, hyperglycemia and advanced glycation end products, elevated prorenin levels, and impaired podocyte-specific insulin signaling – just to name a few!

25
Q

Hypertension

A
  1. Chronic elevations in blood pressure can lead to vascular, glomerular, and tubulointerstitial disease —> hypertensive nephrosclerosis
  2. African Americans – much higher risk of progressive CKD and end-stage-renal-disease (dialysis dependent) despite “adequate” blood pressure control
    a. Association with genetic polymorphisms involving chromosome 22 – apolipoprotein L1 (APOL1) gene
    b. APOL1 is a minor apoprotein component of HDL cholesterol
    c. When intracellular, APOL1 has the ability to kill Trympanosomes that cause African Sleeping Sickness
    d. It is presumed that APOL1 allelic variants confer a selective biological advantage – resistance against Trympanasoma brucei rhodesiense but when inherited in a recessive fashion is associated with both hypertensive CKD with high progression to ESRD (also associated with proteinuria and FSGS in African Americans)
26
Q

Clinical Manifestations Hypertension

A

Patients with hypertensive nephrosclerosis typically have had a long history of hypertension accompanied by retinopathy (vascular changes in the retina due to high arterial pressures), left ventricular hypertrophy, and low-grade proteinuria (<1 g per day)

27
Q

Consequences of CKD

A
  • Cardiovascular Disease
  • Hypertension
  • Mineral Bone Disorder
  • Anemia
28
Q

Cardiovascular Disease

A
  1. Majority of patients with CKD will die from cardiovascular disease rather than progressing to end-stage-renal-disease (ESRD)
  2. Although CKD and cardiovascular disease share many of the same risk factors; even when these variables are factored out, there is an independent risk for developing cardiovascular disease in CKD patients
  3. Both decreased GFR and increase in proteinuria increase the risk of cardiovascular disease
  4. In this study, patients with stage 2-4 CKD were followed over 5 years. Most patients ended up dying from cardiovascular death rather than progressing to ESRD
29
Q

Hypertension

A
  1. Present in 80-85% of patients with CKD 2. Multifactorial including
    a. Sodium retention
    b. Increased activity of the renin-angiotensin system
    c. Enhanced activity of the sympathetic nervous system
    d. Secondary hyperparathyroidism (raises intracellular calcium –> vasoconstriction)
    e. Impaired nitric oxide synthesis and endothelium mediated vasodilitation
30
Q

Mineral Bone Disorder

A
  1. Decreased urinary phosphorus excretion
  2. Compensatory increase in FGF-23 (phosphatonin) increases phosphate excretion in an attempt to maintain normal serum phosphorus concentrations
  3. Decrease in 1,25 Vitamin D (FGF-23 inhibits 1-alph-OH’lase), decrease in serum calcium –> increase in PTH and secondary hyperparathyroidism
  4. Can lead to osteomalacia (soft bones due to defective mineralization), osteitis fibrosa (high bone turnover), and vascular calcification
31
Q

Anemia

A

Decreased erythropoietin production from the kidney

32
Q

Risk Factors for CKD —> ESRD

A
  1. Proteiuria
  2. Hypertension
  3. Type of underlying disease (i.e. diabetes mellitus, polycystic kidney disease)
  4. African-American race
  5. Male gender
  6. Obesity
    a. Increases glomerular capillary pressure
  7. Hyperlipidemia
    a. High lipid levels are associated with a faster rate of progression
  8. Smoking
  9. Hyperphosphatemia
  10. Metabolic acidosis
    a. Bicarbonate supplementation appears to slow progression of CKD
    b. Mechanism thought to be due to reduction in tubulointerstitial inflammation
  11. High protein diet
    a. Increases glomerular capillary pressure
  12. Hyperuricemia
    a. Data emerging that treatment to reduce uric acid levels may slow the rate of GFR loss
33
Q

Interventions That Slow Progression of CKD

A
  1. BP control
  2. Renin-Angiotensin-Aldosterone Antagonism
  3. Control phosphorus levels
  4. Treat metabolic acidosis
  5. Stop smoking!
  6. Correct anemia
  7. Use of an HMG-CoA reductase inhibitor (statin)
  8. Low protein diet
  9. Treat underlying disease
34
Q

BP Control

A

The most important intervention is adequate BP control! •Aim for a goal of <130/80

  • Lower goals have been proposed for patients with overt proteinuria (>1g per day) – i.e. <125/75, but there is no convincing data to support this
  • Recent data suggests lowering BP <140/90 in African Americans has no further beneficial effect
35
Q

Renin-Angiotensin-Aldosterone Antagonism

A
  • Inhibition of angiotensin II and aldosterone (ACE inhibitors, angiotensin receptor blockers) slows progression of CKD in proteinuric diseases (>30mg or albuminuria)
  • Independent of BP lowering effect
  • Decrease glomerular capillary pressure, reduce hyperfiltration, and mitigates tubulointerstitial fibrosis
36
Q

Control Phosphorus Levels

A
  • Dietary discretion
  • Phosphorus binders (taken with meals —> binds phosphorus and eliminates through stool)
37
Q

Treat Metabolic Acidosis

A

•Sodium bicarbonate supplementation (has been shown to slow GFR loss)

38
Q

Correct Anemia

A

•Erythrocyte stimulating agent (ESA) or erythropoietin

39
Q

Use Statins

A

•Associated with slowing of GFR

40
Q

Low Protein Diet

A
  • Benefit primarily in proteinuric diseases (>1g per day) – slows GFR loss
  • Goal ~ 0.6-0.8g/Kg protein per day
  • Should be followed by a nutritionist to avoid malnutrition
41
Q

Treat Underlying Disease

A

• Strict glycemic control in diabetes mellitus

  • Tight control of blood glucose (Hemoglobin A1c <7%) results in improved renal outcomes

• Immunosuppression therapy for primary glomerular diseases (

42
Q

Care of a CKD Patient

A
  • Early referral to a nephrologist
  • Cardiovascular risk modification
  • Prepare for renal replacement therapy
43
Q

Preparation for Renal Replacement Therapy

A

a. Despite our best efforts at employing measure to halt or slow progression of disease, patients will progress to the need of renal replacement therapy
b. Renal replacement therapy is typically needed when GFR drops to ~ 8-15ml/min
c. If symptoms of uremia (nausea, vomiting, anorexia, dysgusia, pruritis or itching, altered sleep habits, impaired cognition, or pericardial effusion), renal replacement therapy should be started regardless of GFR
d. Types of renal replacement therapy
1. In-center hemodialysis
2. Home hemodialysis
3. Peritoneal dialysis
4. Kidney transplant
e. Patients need to be educated about options for renal replacement early
f. Pre-emptive transplant (transplant prior to dialysis) offers the best survival advantage (not always possible)
g. If choosing hemodialysis, a permanent vascular access should be placed at least 12 weeks prior to the need of replacement therapy (i.e. arteriovenous fistula or arteriovenous graft) in order to avoid the use of catheters which carry a higher infectious risk

Renal (26 decks)

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